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A Case For High ROS, Antioxidants Are Useless And Potentially Harmful!

Obi-wan

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Oh, thats a great find! I was trying to understand how normal cells deal with ROS and stumbled upon this:

New Aspects of Mitochondrial Uncoupling Proteins (UCPs) and Their Roles in Tumorigenesis

Apparently highly invasive cancers can deal with ROS in the same manner as healthy cells..

"These data indicated that UCP2-mediated mild mitochondrial uncoupling may serve as a tumor promoting event.
The elevated levels of UCP2 in cancer cells may be a result of long-term selection during tumorigenesis, since any event that results in UCP2 upregulation could help cells escape from apoptosis mediated by the p53 signaling. Given the fact that mitochondrial uncoupling could cause dissipation of the mitochondrial potential, a decrease in mitochondrial ROS, and a reduction in p53’s response to oxidative stress, it is reasonable to propose that mitochondrial uncoupling may provide cancer cells with a prosurvival advantage via suppressing the p53 mediated apoptosis pathway."
 

Obi-wan

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Sulforaphane-induced Cell Death in Human Prostate Cancer Cells Is Initiated by Reactive Oxygen Species

"We have shown previously that sulforaphane (SFN), a constituent of many edible cruciferous vegetables including broccoli, suppresses growth of prostate cancer cells in culture as well as in vivo by causing apoptosis, but the sequence of events leading to cell death is poorly defined. Using PC-3 and DU145 human prostate cancer cells as a model, we now demonstrate, for the first time, that the initial signal for SFN-induced apoptosis is derived from reactive oxygen species (ROS). Exposure of PC-3 cells to growth-suppressive concentrations of SFN resulted in ROS generation, which was accompanied by disruption of mitochondrial membrane potential, cytosolic release of cytochrome c, and apoptosis."

"Because SFN is an electrophilic molecule capable of reacting with cellular nucleophiles, including GSH (35), we reasoned that SFN treatment might cause GSH depletion to exacerbate oxidative stress. We therefore determined the effect of SFN treatment on intracellular levels of GSH by using PC-3 cells, and the results are shown in Fig. 2C. Indeed, SFN treatment caused a rapid decline in the level of GSH. For instance, the GSH levels in PC-3 cells treated for 3 and 6 h with 40 μm SFN were reduced by about 90 and 94%, respectively, compared with control"
 
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haidut

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In Understanding Ray Peat's Model Of Redox

@Mufasa stated

"Ray Peat often write and talks about this, and so does @haidut, but I find this a hard topic to really understand. Many people say that Ray Peat's view about PUFA is the most controversial, but I think his opinion about how redox works is even more controversial. I have been studying this now, and this how I understand it, please feel free to correct me.

The main idea of Ray Peat's model is that as long as the cell is doing oxidative phosphorylation and makes a generous amount of ATP than the cell is healthy and able to withstand many biological problems.

If for some reason, oxidative phosphorylation is impaired, then the cell becomes unhealthy. It could become cancerous, it could become diabetic, it could become lipofuscin etc. etc. Overgeneralizing.

Now the big problem is, how can you make oxidative phosphorylation work again, if it is impaired. Well, oxidative phosphorylation works with a lot of redox reactions. Where high energy molecules/electron donors/reducers give their electrons to low energy molecules/electron acceptors/oxidizers.

Here reducers are molecules such as NADPH, NADH, GSH, vitamin E, vitamin C etc. They often act directly or indirectly as an anti oxidant, as they give their energy to GSH which is the "master antioxidant" that guards against oxidative stress. But they also, when a reducers loses its energy in a redox reaction, they can fuel ADP to ATP, which is the molecule where it is all about. This is the molecule that is needed to keep the cell in a health differentiated gel like state, but also the molecule that the organism needs to meets its energetic demands in the sense of mental and physical activity.

Now oxidants are molecules such as O2, quinones, NAD, MB, ROS. Those are molecules that ask for electrons. Some are highly unstable, such as ROS, which causes oxidative stress.

Now many diseases are marked by oxidative stress, which is why many people believe that you probably need to raise GSH, NADPH, vitamin C, vitamin E etc. to combat those. This would ensure that DNA, membranes, PUFA etc. all don't get damaged from oxidative stress.

However, it is well known that if you want to kill cancer, this is impossible if your anti oxidants are high. Cell apoptosis requires ROS, and anti oxidants neutralize the action of ROS. So many people think that you want high anti oxidants levels, which means a lot of reducers such as NADPH, NADH, GSH, vitamin E etc., except if you have cancer, because otherwise cancer therapies won't be effective in killing it.

Now, here is where Ray Peat differs. He seems to reason that not only in cancer, but everywhere where metabolism is impaired, there is actually a buildup of those electron donors, causing reductive stress. And to restore the flow of molecules, you don't need more of those electron donors, but less, and you need more oxidants, such as O2 (which indirectly means CO2), NAD and quinones, to make sure the electrons start flowing again from donor to acceptor until it fuels ATP, and the cell gets back in its differentiated, gel like state.

Of you course you need reducers for redox, but too much of them seems to impair the enzymes in the mitochondria, too much GSH impairs cytochrome C, too much NAPDH impairs PDH. Ray Peat seems to think that injury, cancer, inflammation has this reductive swarm around it, which impairs metabolism.

Which I think was nicely stated.

Peat thinks that cells are not really damaged. So, there is no damaged metabolic parts to "repair". It is more about cell quorum - the more cells have impared metabolism due to stress and the longer they have been like that the harder it is to snap them out of this. As @tyw and even @Travis mentioned on some other threads, potent "all-clear" signals are provided by thyroid, progesterone, DHEA (in small amounts), pregnenolone, testosterone, emodin, vitamin K/A/E/D, etc. But changing the enviornment is also key and if you continue to be in the same environment that caused the original problem, then it would be more a patch work. That's why Peat said changing the location/environment for even a few days like going on vacation or doing something completely unplanned and unforseen can often change cell quorum in the right direction.
Even without external antioxidants the cell produces its own antioxidant defense system via glutathione (GSH) but then we have Idea labs Pyrucet and I am on Chemo. (high ROS)...plus hypoxia (holding your breath) produces ROS plus exercise (working on that) produces high ROS... I asked @haidut if glucose oxidation produces ROS. I am sure he will say no but the Pyruvate in Pyrucet does and the Acetoacetate limits GSH. So hopefully a game changer...Redox shifts to oxidation. Plus I think the cancer cell produces its own ROS but limits it for signaling via GSH. Haidut was actually amazed on how fast Acetoacetate will bring down GSH to a zero level in a matter of days! Interesting...

Don't know about glucose, but sucrose produces ROS and lowers GSH.
Glycine restores glutathione and protects against oxidative stress in vascular tissue from sucrose-fed rats. - PubMed - NCBI
 

mimmo123

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You need to be able to burn sugar to produce enough co2 if your not producing enough co2 you will get damage
you need to get your co2 high enough and it is hard to do especially keeping it high 24 hours a day

Glucose and sucrose for diabetes.

Increasing the rate of respiration by replacing the fats with glucose reduces the availability of electrons that can trigger lipid peroxidation and produce toxic free radicals, and the shift of fuel also increases the amount of carbon dioxide produced, which can protect the protein amino groups such as lysine from glycation and lipoxidation.
 

Obi-wan

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Peat thinks that cells are not really damaged. So, there is no damaged metabolic parts to "repair". It is more about cell quorum - the more cells have impared metabolism due to stress and the longer they have been like that the harder it is to snap them out of this. As @tyw and even @Travis mentioned on some other threads, potent "all-clear" signals are provided by thyroid, progesterone, DHEA (in small amounts), pregnenolone, testosterone, emodin, vitamin K/A/E/D, etc. But changing the enviornment is also key and if you continue to be in the same environment that caused the original problem, then it would be more a patch work. That's why Peat said changing the location/environment for even a few days like going on vacation or doing something completely unplanned and unforseen can often change cell quorum in the right direction.


Don't know about glucose, but sucrose produces ROS and lowers GSH.
Glycine restores glutathione and protects against oxidative stress in vascular tissue from sucrose-fed rats. - PubMed - NCBI

Glycine is a big NO for a cancer patient. That's why I feel worse when I have a large bowl of soup. I believe cancer cells have a definite defect in metabolism and must be stopped from multiplying and must be destroyed. They rely on the antioxidant system to escape death and use the mROS for signaling and multiplication. That's why creating a high mROS environment and diminishing GSH makes so much sense. In Physiological roles of mitochondrial reactive oxygen species

"Following review of the divergent biological processes that are regulated by mROS, we can make some generalizations regarding the induction and function of mROS. Importantly, mROS are generally induced by cell stress – hypoxia, starvation, pathogen infection (or molecular harbingers of pathogen infection), and growth factor stimulation. Thus, mROS are poised to serve as an alarm to notify the cell that the extracellular environment is changing. This mROS alarm system is titrated such that the gravity of the stressor correlates with the quantity of mROS induced – a stressor that is incompatible with cell viability induces larger quantities of mROS, which nonspecifically produce cell damage and subsequent cell death, while a moderate stressor induces smaller quantities of mROS (Figure 4). As we have described, these small inductions of mROS promote adaptation to the stressor – HIF activation under hypoxia, autophagy activation under starvation, inflammatory cytokine production under pathogen infection, differentiation under receptor dependent stimulation – and consequently promote cell survival."

Cancer cells are smart and have figured out how to adapt and survive. We must be smarter and understand what enzymes to manipulate to promote cancer cell death...
 
B

Braveheart

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Glycine is a big NO for a cancer patient. That's why I feel worse when I have a large bowl of soup. I believe cancer cells have a definite defect in metabolism and must be stopped from multiplying and must be destroyed. They rely on the antioxidant system to escape death and use the mROS for signaling and multiplication. That's why creating a high mROS environment and diminishing GSH makes so much sense. In Physiological roles of mitochondrial reactive oxygen species

"Following review of the divergent biological processes that are regulated by mROS, we can make some generalizations regarding the induction and function of mROS. Importantly, mROS are generally induced by cell stress – hypoxia, starvation, pathogen infection (or molecular harbingers of pathogen infection), and growth factor stimulation. Thus, mROS are poised to serve as an alarm to notify the cell that the extracellular environment is changing. This mROS alarm system is titrated such that the gravity of the stressor correlates with the quantity of mROS induced – a stressor that is incompatible with cell viability induces larger quantities of mROS, which nonspecifically produce cell damage and subsequent cell death, while a moderate stressor induces smaller quantities of mROS (Figure 4). As we have described, these small inductions of mROS promote adaptation to the stressor – HIF activation under hypoxia, autophagy activation under starvation, inflammatory cytokine production under pathogen infection, differentiation under receptor dependent stimulation – and consequently promote cell survival."

Cancer cells are smart and have figured out how to adapt and survive. We must be smarter and understand what enzymes to manipulate to promote cancer cell death...
I finally understand the ROS role...good post and link...thank you for your persistence and sharing.
 

Obi-wan

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Braveheart

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Found these two studies of interest:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC124244/pdf/pq1102007408.pdf

"VES, an esterified vitamin E analog, has little antioxidant activity"

VES is Vit E Succinate

https://www.researchgate.net/public..._growth_and_survival_of_prostate_cancer_cells

"Vitamin E succinate (VES), the most potent derivative of vitamin E for anti-
tumor activity"
https://www.vitacost.com/nutricolog...sules?q=vitamin+e+succinate&ta=VITAMIN+E+SUCC
Mine...does it pass muster?
 

Obi-wan

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This study was sponsored by the U.S. Army Medical Research and Materiel Command, Fort Detrick, Maryland 21702-5012

https://apps.dtic.mil/dtic/tr/fulltext/u2/a545657.pdf

CONCLUSIONS:
Benzimidazoles were identified from a screen that selectively target highly metastatic prostate cancer cells but not toxic to normal cells. We determined that the preferential antitumor activity of these agents was mediated partly through cell cycle arrest and induction of apoptosis, both in vitro and in vivo. We further demonstrate that benzimidazole treatment prolongs the survival of mice bearing prostate cancer lung metastases and inhibit the growth of prostate cancer cells growing in the bone microenvironment. More strikingly, these anti-tumor effects remain active against prostate cancer cells that are resistant to paclitaxel, the standard chemotherapy for men with advanced prostate cancer, both in vitro as well as in vivo. Our study further supports the use of benzimidazoles as potential anti-cancer therapy for men with metastatic prostate cancer.

On my second week of Fenbendazole now with daily 800 iu of Vit E Succinate plus Taxatore every three weeks for 6 sessions. Thursday is number 3. This study was done on May 2011 and shows you what a REAL study looks like! It doesn't get better than this! I love the fact that Vit. E Succinate does not act like an antioxidant and is the most potent derivative of vitamin E for anti-tumor activity. The "zoles" are unbelievable for anti-cancer activity!
 
B

Braveheart

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This study was sponsored by the U.S. Army Medical Research and Materiel Command, Fort Detrick, Maryland 21702-5012

https://apps.dtic.mil/dtic/tr/fulltext/u2/a545657.pdf

CONCLUSIONS:
Benzimidazoles were identified from a screen that selectively target highly metastatic prostate cancer cells but not toxic to normal cells. We determined that the preferential antitumor activity of these agents was mediated partly through cell cycle arrest and induction of apoptosis, both in vitro and in vivo. We further demonstrate that benzimidazole treatment

prolongs the survival of mice bearing prostate cancer lung metastases and inhibit the growth of prostate cancer cells growing in the bone microenvironment. More strikingly, these anti-tumor effects remain active against prostate cancer cells that are resistant to paclitaxel, the standard chemotherapy for men with advanced prostate cancer, both in vitro as well as in vivo. Our study further supports the use of benzimidazoles as potential anti-cancer therapy for men with metastatic prostate cancer.

On my second week of Fenbendazole now with daily 800 iu of Vit E Succinate plus Taxatore every three weeks for 6 sessions. Thursday is number 3. This study was done on May 2011 and shows you what a REAL study looks like! It doesn't get better than this! I love the fact that Vit. E Succinate does not act like an antioxidant and is the most potent derivative of vitamin E for anti-tumor activity. The "zoles" are unbelievable for anti-cancer activity!

You're gonna win it....
 

Obi-wan

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Another great study on Fenbendazole at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3436308/

"In recent years, there has been a great deal of interest in proteasome inhibitors as a novel class of anticancer drugs. We report that fenbendazole (FZ) (methyl N-(6-phenylsulfanyl-1H-benzimidazol-2-yl)carbamate) exhibits a potent growth-inhibitory activity against cancer cell lines but not normal cells"

"We then compared the antiproliferative ability of FZ with other established anticancer drugs. The results of a time-dependent growth assay clearly indicated FZ to be a more effective cytotoxic agent as compared with cisplatin and taxol"

"Altogether, our results indicate that FZ induces cytotoxicity in cancer cells via impairment of proteasome function and induction of unfolded protein response."

"Therefore, we propose FZ as a novel drug candidate that targets the ubiquitin-proteasome pathway and effectively kills cancer cells."

"FZ-induced ROS generation could be associated with the transcriptional activation of ROS-related genes. Our data show PIG3 induction upon FZ treatment. PIG3 is a p53-inducible gene homolog of oxidoreductase and is reported to be associated with p53-induced elevation of ROS production(51)."
 

Obi-wan

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Back to a case for antioxidants Antioxidants and Cancer Risk: The Good, the Bad, and the Unknown

"As more recent studies continue to suggest antioxidants could actually help cancer cells grow, research by Zachary Schafer shows that cancer cells’ survival can be aided by antioxidants that protect these cells from free radicals.10 Free radicals harm cells, and getting rid of free radicals therefore can help cancer cells. “If you are a person who is healthy, meaning no tumors of any kind, antioxidants are probably going to protect against cancer,” Schafer says. But he points out that if a person has cancer cells, antioxidants can help those cancer cells survive."
 

Obi-wan

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TreasureVibe

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Sodium selenite supposedly kills cancer cells through oxidation according to studies, if this is the correct way of describing its action. Correct me if I am wrong.

It is only a specific sodium selenite that has anticancer activity according to one of the studies under, quote:

"However, it is now firmly established that only an inorganic sodium selenite with four-valent Se, and not that with six-valent (selenate) cation shows anticancer activity."

Sodium Selenite as an Anticancer Agent. - PubMed - NCBI
Application of Sodium Selenite in the Prevention and Treatment of Cancers
Rationale for the treatment of cancer with sodium selenite. - PubMed - NCBI
https://www.google.com/url?sa=t&sou...Vaw3vwvD_gA96AWVsm_ihEoRF&cshid=1554620194017 (Document download from university)
https://www.sciencedirect.com/science/article/pii/S0946672X1630075X
Selenite-induced autophagy antagonizes apoptosis in colorectal cancer cells in vitro and in vivo
https://www.researchgate.net/publication/303893204_Sodium_Selenite_as_an_Anti-Cancer_Agent
Sodium Selenite Benefits Are Numerous
https://www.hindawi.com/journals/omcl/2016/4741694/
https://www.google.com/url?sa=t&sou...WMAJ6BAgJEAE&usg=AOvVaw0COeJ0ZlqWb5fNuEI9zEEd (downloadable document Chinese study)
Sodium Selenite Induces Superoxide-Mediated Mitochondrial Damage and Subsequent Autophagic Cell Death in Malignant Glioma Cells
Sodium selenite induces apoptosis in colon cancer cells via Bax-dependent mitochondrial pathway
Combined effect of sodium selenite and docetaxel on PC3 metastatic prostate cancer cell line | Estudo Geral
Effect of Sodium Selenite on Gene Expression of SELF, SELW, and TGR Selenoproteins in Adenocarcinoma Cells of the Human Prostate
https://www.redjournal.org/article/S0360-3016(10)00409-8/pdf
https://pubs.rsc.org/en/Content/ArticleLanding/2013/MT/c3mt00002h#!divAbstract
https://www.google.com/url?sa=t&sou...WMAV6BAgAEAE&usg=AOvVaw1cXNRiJrukr87GvSMLvUqb (downloadable document study)
http://europepmc.org/abstract/MED/18405881
https://jhoonline.biomedcentral.com/articles/10.1186/1756-8722-6-7
https://www.google.com/url?sa=t&sou...WMAh6BAgCEAE&usg=AOvVaw3bunZz7Lz5Bc6AoyYx-E2M (downloadable document study, sodium selenite reverses chemotherapy resistance in cancer study)

"Sodium Selenite

Sodium selenite destroys cancer cells by selectively generating toxic free radicals (reactive oxygen species) which target the destruction of the mitochondria in cancer cells, however not in healthy cells.

Sodium selenite helps with the repair of damaged genes (DNA segments). This reduces the risk of new cancers being formed.

Numerous human studies with sodium selenite support the use of this form of selenium as a possible additional treatment for cancer patients and for preventing new or recurring cases of cancer.

In a randomized controlled clinical trial of sodium selenite using 200 mcg per day versus a placebo in patients with aggressive head and neck cancers, patients given the supplement showed an increased ability to destroy cancer cells. In another study it was shown that temporary use of 1,000 mcg of sodium selenite in patients with oral tumors effectively reduced potentially deadly swelling in these patients after surgery. Sodium selenite in patients with newly diagnosed non-Hodgkin's lymphoma increased the response rate to chemotherapy by 50% compared to a placebo group, and significantly increased overall survival time."

Source: https://www.liverdoctor.com/selenium-cancer-fighting-mineral/

And there's many more information, studies and literature to be found on sodium selenite for cancer on the internet. Hope this helps.
 
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Obi-wan

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Sodium selenite supposedly kills cancer cells through oxidation according to studies, if this is the correct way of describing its action. Correct me if I am wrong.

It is only a specific sodium selenite that has anticancer activity according to one of the studies under, quote:

"However, it is now firmly established that only an inorganic sodium selenite with four-valent Se, and not that with six-valent (selenate) cation shows anticancer activity."

Sodium Selenite as an Anticancer Agent. - PubMed - NCBI
Application of Sodium Selenite in the Prevention and Treatment of Cancers
Rationale for the treatment of cancer with sodium selenite. - PubMed - NCBI
https://www.google.com/url?sa=t&source=web&rct=j&url=https://www.adelaide.edu.au/directory/graham.lyons?dsn=directory.file;field=data;id=19832;m=view&ved=2ahUKEwjNucaSsr3hAhVBYlAKHdXzBbAQFjADegQIARAB&usg=AOvVaw3vwvD_gA96AWVsm_ihEoRF&cshid=1554620194017 (Document download from university)
https://www.sciencedirect.com/science/article/pii/S0946672X1630075X
Selenite-induced autophagy antagonizes apoptosis in colorectal cancer cells in vitro and in vivo
https://www.researchgate.net/publication/303893204_Sodium_Selenite_as_an_Anti-Cancer_Agent
Sodium Selenite Benefits Are Numerous
https://www.hindawi.com/journals/omcl/2016/4741694/
https://www.google.com/url?sa=t&sou...WMAJ6BAgJEAE&usg=AOvVaw0COeJ0ZlqWb5fNuEI9zEEd (downloadable document Chinese study)
Sodium Selenite Induces Superoxide-Mediated Mitochondrial Damage and Subsequent Autophagic Cell Death in Malignant Glioma Cells
Sodium selenite induces apoptosis in colon cancer cells via Bax-dependent mitochondrial pathway
Combined effect of sodium selenite and docetaxel on PC3 metastatic prostate cancer cell line | Estudo Geral
Effect of Sodium Selenite on Gene Expression of SELF, SELW, and TGR Selenoproteins in Adenocarcinoma Cells of the Human Prostate
https://www.redjournal.org/article/S0360-3016(10)00409-8/pdf
Comparative proteomics analysis of sodium selenite-induced apoptosis in human prostate cancer cells - Metallomics (RSC Publishing)
https://www.google.com/url?sa=t&sou...WMAV6BAgAEAE&usg=AOvVaw1cXNRiJrukr87GvSMLvUqb (downloadable document study)
Treatment of lung cancer cells with cytotoxic levels of sodium selenite: effects on the... - Abstract - Europe PMC
https://jhoonline.biomedcentral.com/articles/10.1186/1756-8722-6-7
https://www.google.com/url?sa=t&sou...WMAh6BAgCEAE&usg=AOvVaw3bunZz7Lz5Bc6AoyYx-E2M (downloadable document study, sodium selenite reverses chemotherapy resistance in cancer study)

"Sodium Selenite

Sodium selenite destroys cancer cells by selectively generating toxic free radicals (reactive oxygen species) which target the destruction of the mitochondria in cancer cells, however not in healthy cells.

Sodium selenite helps with the repair of damaged genes (DNA segments). This reduces the risk of new cancers being formed.

Numerous human studies with sodium selenite support the use of this form of selenium as a possible additional treatment for cancer patients and for preventing new or recurring cases of cancer.

In a randomized controlled clinical trial of sodium selenite using 200 mcg per day versus a placebo in patients with aggressive head and neck cancers, patients given the supplement showed an increased ability to destroy cancer cells. In another study it was shown that temporary use of 1,000 mcg of sodium selenite in patients with oral tumors effectively reduced potentially deadly swelling in these patients after surgery. Sodium selenite in patients with newly diagnosed non-Hodgkin's lymphoma increased the response rate to chemotherapy by 50% compared to a placebo group, and significantly increased overall survival time."

Source: https://www.liverdoctor.com/selenium-cancer-fighting-mineral/

And there's many more information, studies and literature to be found on sodium selenite for cancer on the internet. Hope this helps.


This is very interesting as I had stopped taking Selenomethionine due to it being an antioxidant. So now we know that inorganic Selenite is not an antioxidant but possesses oxidizing properties.

In the study at https://estudogeral.sib.uc.pt/bitst...ncer cell line(BiochemBiophysREsComm2011).pdf

"Docetaxel and sodium selenite inhibit prostate cancer cells
(PC3) growth in a dose and time dependent-manner.
Half maximal inhibitory concentration values (IC50) of docetaxel
(Fig. 1A) and sodium selenite (Fig. 1B) were reached for
approximately 500 nM (Rsqr: 0.998) and 10 lM (Rsqr: 0.991),
respectively, after 24 h incubation. However, when we treat the
cells with 100 nM docetaxel and 2.5 lM sodium selenite simultaneously,
we observed a synergistic antiproliferative effect
(Fig. 1C). In fact, sodium selenite and docetaxel combination have
a synergistic effect on cell growth inhibition (67%) compared with
docetaxel (22%) and sodium selenite (24%) alone."

"On the other hand cell death may be related with oxidative
stress induction. In fact docetaxel has been recently associated to
an increase of ROS in the prostate cancer DU-145 cells [27]. Surprisingly,
we found ROS depletion after 24 h treatment (Fig. 4).
Moreover, it could be a result of peroxides conversion into hydroxyl
radicals. However, data not shown indicate that sodium selenite
and docetaxel alone, or in combination, did not interfere on
PC3 peroxides production after 6 h treatment. Therefore, we admit
that sodium selenite could inhibit the antioxidant system leading
to oxidative lesion by reactive hydroxyl radicals and consequent
cell death."

"Reduced glutathione (GSH), counteract oxidative stress by directly
quenching reactive oxygen species and has been associated
to resistance to apoptosis and radiation in prostate cancer cells
[28]. Besides sodium selenite supplies selenium for synthesis of seleno-
proteins such as the antioxidant defenses glutathione peroxidase
(Gl-Px) and thioredoxin reductase, higher concentrations are
related with increased oxidative stress by decreasing reduced glutathione/
oxidized glutathione (GSH/GSSG) ratio and also by altering
MnSOD subcellular distribution. These observations are
related with an increase of ROS levels and cell sensitization to
apoptosis [13–15,29]."
 

Inaut

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@Obi-wan As per travis—-I thought the benefit of selenomethionine wasn’t necessarily it’s role as an anti-oxidant/oxidant in cancer proliferation but rather it’s effect on inhibiting polyamine synthesis??

The more I read the more I become confused

“I think it depends on the person because they have different pharmacokinetics. It has been shown that selenomethionine is four times more effective than selenide for preventing pancreatic degeneration in chicks,⁽¹⁾ perhaps indicating that the pancreatic membranes are highly lipophilic and largely-exclude the water-soluble selenide (or perhaps selenide gets absorbed to far-up the digestive tract; selenomethionine further down). Selenide does seem to reach many body locations quicker, but since the prostate has such a high methionine requirement—for polyamine synthesis—selenomethionine would likely be the better choice for reaching that.”
 
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